Acute Liver Failure Mouse Model Lineup

Acute liver failure (ALF) carries a high mortality of approximately 40%, which is caused by virus infections (hepatitis A, B and E), drug-induced liver injury (acetaminophen/paracetamol) or autoimmune hepatitis. ALF exhibits symptoms of severe injury such as destruction of hepatocytes or decrease in liver function due to massive necrosis and inflammation.


We have lineup of models that can be widely used in studies on the mechanisms of acute liver injury and liver regeneration, as well as in drug efficacy evaluation studies.


  • CCl4-induced acute liver failure model
    The CCl4 model is a widely used model for research on the mechanisms of acute liver injury (such as dysbolism, inflammation, necrosis) and the development of new drugs. Highly reactive radical species are produced as metabolites, causing hepatocyte necrosis via lipid peroxidation and cell membrane damage.
  • Concanavalin A (ConA)-induced autoimmune hepatitis
    The ConA model is used for autoimmune hepatitis, which is primarily driven by the activation and recruitment of T cells to the liver. The outcome of ConA-induced ALF is severe liver inflammation, tissue necrosis and terminal organ failure.
  • Thioacetamide (TAA)-induced drug-induced liver injury model
    The TAA model is a classic liver injury model. While TAA itself is not hepatotoxic, its reactive metabolites covalently bind to proteins and lipids, thereby causing oxidative stress, inflammation and centrilobular necrosis.
  • Acetaminophen (APAP)-induced drug-induced liver injury model

    The APAP model is used as a model of acute liver failure due to APAP overdose. Excess APAP causes an increase in highly toxic metabolic intermediates (Known as NAPQI) that arise during drug metabolism in the liver, leading to necrosis of hepatocytes.

  • LPS/D-GalN-induced acute liver injury model
    The D-gal/LPS model is made by administrating a combination of D-galactosamine and lipopolysaccharide leading to more rapid and efficient disease induction. D-gal/LPS induces a robust inflammation and apoptosis via immune response.


We are always happy to tailor each study to fit the requirements and needs of the client.

We would be honored to use our many years of experience, as well as our expertise in the areas of inflammation and fibrosis, to assist you with your study.


If what you saw today looked interesting, please feel free to contact us with questions or concerns.

If you would like more information regarding our services or what models we offer, please don’t hesitate to reach out.